scholarly journals Editorial: Mitochondria at the Crossroads of Immunity and Inflammatory Tissue Damage

2021 ◽  
Vol 12 ◽  
Author(s):  
João Paulo Silva Nunes ◽  
Pedro M. Moraes-Vieira ◽  
Christophe Chevillard ◽  
Edecio Cunha-Neto
2009 ◽  
Vol 425 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Valdecir F. Ximenes ◽  
Ghassan J. Maghzal ◽  
Rufus Turner ◽  
Yoji Kato ◽  
Christine C. Winterbourn ◽  
...  

During inflammatory events, neutrophils and platelets interact to release a variety of mediators. Neutrophils generate superoxide and hydrogen peroxide, and also discharge the haem enzyme myeloperoxidase. Among numerous other mediators, platelets liberate serotonin (5-hydroxytryptamine), which is a classical neurotransmitter and vasoactive amine that has significant effects on inflammation and immunity. In the present study, we show that serotonin is a favoured substrate for myeloperoxidase because other physiological substrates for this enzyme, including chloride, did not affect its rate of oxidation. At low micromolar concentrations, serotonin enhanced hypochlorous acid production by both purified myeloperoxidase and neutrophils. At higher concentrations, it almost completely blocked the formation of hypochlorous acid. Serotonin was oxidized to a dimer by myeloperoxidase and hydrogen peroxide. It was also converted into tryptamine-4,5-dione, especially in the presence of superoxide. This toxic quinone was produced by stimulated neutrophils in a reaction that required myeloperoxidase. In plasma, stimulated human neutrophils oxidized serotonin to its dimer using the NADPH oxidase and myeloperoxidase. We propose that myeloperoxidase will oxidize serotonin at sites of inflammation. In doing so, it will impair its physiological functions and generate a toxic metabolite that will exacerbate inflammatory tissue damage. Consequently, oxidation of serotonin by myeloperoxidase may profoundly influence inflammatory processes.


2010 ◽  
Vol 69 (Suppl 2) ◽  
pp. A19-A20
Author(s):  
C Cromme ◽  
L H Meyer ◽  
K Neugebauer ◽  
A Korb ◽  
C Wunrau ◽  
...  

2002 ◽  
Vol 23 (2) ◽  
pp. 61-64 ◽  
Author(s):  
Tom E Mollnes ◽  
Wen-Chao Song ◽  
John D Lambris

2021 ◽  
Author(s):  
Evgeniya V Shmeleva ◽  
Mercedes Gomez de Agüero ◽  
Josef Wagner ◽  
Anton J Enright ◽  
Andrew J Macpherson ◽  
...  

Interactions between pathogens, host microbiota and the immune system influence many physiological and pathological processes. In the 20 th century, widespread dermal vaccination with vaccinia virus (VACV) led to the eradication of smallpox but how VACV interacts with the microbiota and whether this influences the efficacy of vaccination are largely unknown. Here we report that intradermal vaccination with VACV induces a large increase in the number of commensal bacteria in infected tissue, which enhance recruitment of inflammatory cells, promote tissue damage and increase immunity. Treatment of vaccinated specific-pathogen-free (SPF) mice with antibiotic, or infection of genetically-matched germ-free (GF) animals caused smaller lesions without alteration in virus titre. Tissue damage correlated with enhanced neutrophil and T cell infiltration and levels of pro-inflammatory tissue cytokines and chemokines. One month after vaccination, GF mice had reduced VACV-neutralising antibodies compared to SPF mice; while numbers of VACV-specific CD8 + T cells were equal in all groups of animals. Thus, skin microbiota may provide an adjuvant-like stimulus during vaccination with VACV. This observation has implications for dermal vaccination with live vaccines.


Brain ◽  
2007 ◽  
Vol 130 (8) ◽  
pp. 2186-2198 ◽  
Author(s):  
S. Nessler ◽  
S. Boretius ◽  
C. Stadelmann ◽  
A. Bittner ◽  
D. Merkler ◽  
...  

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